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Macrophage‐Specific Deletion of Zxdb Protects Against Sepsis‐Induced Acute Kidney Injury. (A) Generation strategy for myeloid‐specific Zxdb knockout (Mac‐Zxdb‐KO) mice. (B) H&E staining of kidney sections from Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice. (C‐D) Serum creatinine (Scr) (C) and blood urea nitrogen (BUN) (D) levels in Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice at 24 h post‐CLP. <t>(E)</t> <t>KIM‐1</t> immunohistochemistry of kidney sections from Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice. (F) TUNEL staining of kidney sections from Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice. (G) Immunofluorescence of kidney sections stained for F480, CD86, and CD206. (H) Serum IL‐1β, IL‐10, and TNF‐α levels in Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice at 24 h post‐CLP. * p < 0.05, ** p < 0.01, *** p < 0.001.
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Macrophage‐Specific Deletion of Zxdb Protects Against Sepsis‐Induced Acute Kidney Injury. (A) Generation strategy for myeloid‐specific Zxdb knockout (Mac‐Zxdb‐KO) mice. (B) H&E staining of kidney sections from Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice. (C‐D) Serum creatinine (Scr) (C) and blood urea nitrogen (BUN) (D) levels in Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice at 24 h post‐CLP. <t>(E)</t> <t>KIM‐1</t> immunohistochemistry of kidney sections from Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice. (F) TUNEL staining of kidney sections from Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice. (G) Immunofluorescence of kidney sections stained for F480, CD86, and CD206. (H) Serum IL‐1β, IL‐10, and TNF‐α levels in Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice at 24 h post‐CLP. * p < 0.05, ** p < 0.01, *** p < 0.001.
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Macrophage‐Specific Deletion of Zxdb Protects Against Sepsis‐Induced Acute Kidney Injury. (A) Generation strategy for myeloid‐specific Zxdb knockout (Mac‐Zxdb‐KO) mice. (B) H&E staining of kidney sections from Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice. (C‐D) Serum creatinine (Scr) (C) and blood urea nitrogen (BUN) (D) levels in Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice at 24 h post‐CLP. <t>(E)</t> <t>KIM‐1</t> immunohistochemistry of kidney sections from Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice. (F) TUNEL staining of kidney sections from Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice. (G) Immunofluorescence of kidney sections stained for F480, CD86, and CD206. (H) Serum IL‐1β, IL‐10, and TNF‐α levels in Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice at 24 h post‐CLP. * p < 0.05, ** p < 0.01, *** p < 0.001.
Anti Kim 1, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech antibodies against kim 1
RBM3 overexpression ameliorates renal function and histopathological damage in rats at 48 h after burns. (A) HE staining of renal tissue. Scale bar = 100 μm, 50 μm. (B) Immunofluorescence detection of kidney injury molecule <t>KIM‐1.</t> Scale bar = 100 μm. (C) Quantitative results shows the decreased KIM‐1 expression by RBM3 OE. (D) Renal function test results suggests the reduced CREA level by RBM3 OE. (E) Renal function test results suggests the decreased UREA level by RBM3 OE. (* p < 0.05 vs. Control, # p < 0.05 vs. AKI, & indicates p < 0.05 vs. AKI + RBM3 NC).
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RBM3 overexpression ameliorates renal function and histopathological damage in rats at 48 h after burns. (A) HE staining of renal tissue. Scale bar = 100 μm, 50 μm. (B) Immunofluorescence detection of kidney injury molecule <t>KIM‐1.</t> Scale bar = 100 μm. (C) Quantitative results shows the decreased KIM‐1 expression by RBM3 OE. (D) Renal function test results suggests the reduced CREA level by RBM3 OE. (E) Renal function test results suggests the decreased UREA level by RBM3 OE. (* p < 0.05 vs. Control, # p < 0.05 vs. AKI, & indicates p < 0.05 vs. AKI + RBM3 NC).
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Image Search Results


Macrophage‐Specific Deletion of Zxdb Protects Against Sepsis‐Induced Acute Kidney Injury. (A) Generation strategy for myeloid‐specific Zxdb knockout (Mac‐Zxdb‐KO) mice. (B) H&E staining of kidney sections from Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice. (C‐D) Serum creatinine (Scr) (C) and blood urea nitrogen (BUN) (D) levels in Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice at 24 h post‐CLP. (E) KIM‐1 immunohistochemistry of kidney sections from Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice. (F) TUNEL staining of kidney sections from Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice. (G) Immunofluorescence of kidney sections stained for F480, CD86, and CD206. (H) Serum IL‐1β, IL‐10, and TNF‐α levels in Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice at 24 h post‐CLP. * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: The FASEB Journal

Article Title: ZXDB Drives Macrophage Inflammatory Programming in Sepsis‐Induced Acute Kidney Injury by Recruiting EIF4A3 to Enhance ACACA Translation

doi: 10.1096/fj.202502962RR

Figure Lengend Snippet: Macrophage‐Specific Deletion of Zxdb Protects Against Sepsis‐Induced Acute Kidney Injury. (A) Generation strategy for myeloid‐specific Zxdb knockout (Mac‐Zxdb‐KO) mice. (B) H&E staining of kidney sections from Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice. (C‐D) Serum creatinine (Scr) (C) and blood urea nitrogen (BUN) (D) levels in Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice at 24 h post‐CLP. (E) KIM‐1 immunohistochemistry of kidney sections from Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice. (F) TUNEL staining of kidney sections from Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice. (G) Immunofluorescence of kidney sections stained for F480, CD86, and CD206. (H) Serum IL‐1β, IL‐10, and TNF‐α levels in Sham, WT SI‐AKI, and Mac‐Zxdb‐KO SI‐AKI mice at 24 h post‐CLP. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Sections were blocked and incubated overnight at 4°C using primary antibody against KIM‐1 (AF1817; R&D Systems, 1:200).

Techniques: Knock-Out, Staining, Immunohistochemistry, TUNEL Assay, Immunofluorescence

RBM3 overexpression ameliorates renal function and histopathological damage in rats at 48 h after burns. (A) HE staining of renal tissue. Scale bar = 100 μm, 50 μm. (B) Immunofluorescence detection of kidney injury molecule KIM‐1. Scale bar = 100 μm. (C) Quantitative results shows the decreased KIM‐1 expression by RBM3 OE. (D) Renal function test results suggests the reduced CREA level by RBM3 OE. (E) Renal function test results suggests the decreased UREA level by RBM3 OE. (* p < 0.05 vs. Control, # p < 0.05 vs. AKI, & indicates p < 0.05 vs. AKI + RBM3 NC).

Journal: The FASEB Journal

Article Title: Augmenting the Endogenous RBM3 Response Protects Against Burn‐Induced Acute Kidney Injury by Enhancing Macrophage‐Mediated Resolution of Inflammation

doi: 10.1096/fj.202503604RR

Figure Lengend Snippet: RBM3 overexpression ameliorates renal function and histopathological damage in rats at 48 h after burns. (A) HE staining of renal tissue. Scale bar = 100 μm, 50 μm. (B) Immunofluorescence detection of kidney injury molecule KIM‐1. Scale bar = 100 μm. (C) Quantitative results shows the decreased KIM‐1 expression by RBM3 OE. (D) Renal function test results suggests the reduced CREA level by RBM3 OE. (E) Renal function test results suggests the decreased UREA level by RBM3 OE. (* p < 0.05 vs. Control, # p < 0.05 vs. AKI, & indicates p < 0.05 vs. AKI + RBM3 NC).

Article Snippet: The sections were then incubated overnight at 4°C with primary antibodies against KIM‐1 (Proteintech, 30948‐1‐AP, 1:200), CD86 (Bioss, bs‐43589R, 1:200), CD206 (Affinity, DF4149, 1:200), F4/80 (1:200), and Caspase‐3 (1:200).

Techniques: Over Expression, Staining, Immunofluorescence, Expressing, Control